Low back pain (LBP) is a multifactorial issue that is prevalent across most human populations, westernised, rural and indigenous. Deconditioning of the lumbar extensor musculature is a commonly associated factor and has been shown prospectively to be a risk factor for development of LBP. Here an explanation concerning lumbar spine and pelvic anatomic evolution is offered in attempt to integrate these findings. It appears that anatomically modern humans may be predisposed to LBP as a consequence of their evolutionary heritage; the compromise of relatively strong hip/trunk extensors and relatively weak lumbar extensors in combination with a long flexible lumbar spine.

1. An Ancient Perspective on
Deconditioning in Low Back Pain
James Steele

2. Outline of Presentation
• What is Low Back Pain (LBP)?
– Prevalence & Costs
– Multifactorial Model
– Deconditioning
• An Evolutionary Hypothesis
– Development of the Hypothesis
• Traditional Populations
• Role of the Lumbar Spine in Gait
• The Emergence of Bipedalism
• Changes in Lumbar/Pelvic Structure
• Changes in Lumbar/Hip Musculature
– Conceptualising the Hypothesis
• Problems with the Hypothesis
• What it Could Explain
• What it Would Predict
• Conclusions

3. What is Low Back Pain (LBP)?
• NICE1 describes as LBP “…tension, soreness and/or
stiffness in the lower back region…”
• ‘Non-specific’
– “…for which it is not possible to identify a
specific cause of pain.” (pp. 4.)
• Acute/Sub-Acute/Chronic2
– Natural History Myth – “…chronic back pain
always starts as acute back pain.” 3
– 69-75% of acute LBP develops into chronic
LBP4,5
– Increasing frequency and severity6

4. • Multi-factorial with many physical symptoms
– Associated symptoms include (but not limited to):
• Limited lumbar range of motion (ROM)7,8
• Abhorrent gait9-18
• Degenerated AND/OR diseased AND/OR injured intervertebral
discs19-30
• A range of ‘potential’ pain sources1,31,32
– Including (but not limited to):
• Facet joints33,34
• Intervertebral discs35,36
• Ligamentous tissues 37
• However, it is difficult to determine exact source of pain
• As much as 85% of cases are labelled ‘non-specific’ 38

5. Prevalence and Costs
• Prevalence39
– Point prevalence -12-33%
– Year prevalence -22-65%
– Lifetime prevalence - 11-84%
– LBP, CLBP and recurrent LBP40
• Costs –
– ~£5 to £10 billion41,42
– ~$100 to $200 billion43
• Direct (treatments, care etc.)
– £1632 million41
• Indirect (Working losses etc.)
– ~84% - 93% of total costs44,45
– UK ~50 millions working days42
– US ~149 million working days46
• Sickness & Invalidity?
– Prevalence has not changed (or only
slightly)
• UK - 1971 to 2008 similar47-49
• US - 1992 to 2006 +6.3%50
– Sickness and Invalidity
• UK – 1988 to 1998 sharp
increase48
• US – 1987 to 1995 -34%51

6. Multifactorial Model
Figure 1. Integrated model of function considering presenting symptoms of
LBP adpated from Lee & Vleeming52

7. Deconditioning as a Risk Factor
• Disuse or Deconditioning?
– ‘Disuse’ (i.e. a decrease in physical
activity levels)
• Activity levels not different
between asymptomatic and
CLBP53
• Activity levels do not change
with CLBP54
• Does not consider first
injury/LBP
– ‘Deconditioning’ (i.e. a decrease in
function)
• Often not defined (i.e. Reduced
activity levels,
cardiovascular/aerobic fitness
and muscular
strength/endurance
• Thus, reviews suggest it is not
present55-58
Figure 2. Deconditoning syndrome model – Adapted Disuse Syndrome
Model with addition of initial injury, adapted from Verbunt et al.55

8. Lets be More Specific
• Strength/Endurance of the Trunk not associated with LBP55-58
– But ‘Trunk’ Function Includes:
• Hip function
• AND
• Lumbar function
• Lumbar Extension
– Erector Spinae & Lumbar Multifidus
• Vary in contribution but both fundamental
to spinal stability59-69
• Strength/endurance testing of lumbar extensor
musculature,
• Imaging and histochemical examination of the
lumbar extensor musculature
• Fatigue testing of the lumbar extensor musculature
using electromyography

9. Evidence for Lumbar Extensor
Deconditioning
• Cross sectional (i.e. difference between asymptomatic and symptomatic)
– Strength/endurance testing of lumbar extensor musculature,
• Trunk extension studies inconsistent
– Symptomatic sig. weaker70-92
– No Diff. 76,79,81,82,91,93-100
• Isolated lumbar extension
– Symptomatic sig. weaker101-107
– One exception108
– Imaging and histochemical examination of the lumbar extensor musculature
• Imaging studies
– Symptomatic sig. Greater atrophy84,109-111
– No adverse fibre type87
– Fatigue testing of the lumbar extensor musculature using electromyography
– Symptomatic sig. Greater fatigability89,112,113
– No Diff.87,98

10. • Prospective (i.e. baseline factors associated with first time LBP)
– Mixed methodologies
– Most suggestive78,94,114-120
• Austin Bradford-Hill criteria121
– Biological plausibility
– Consistent association
– Temporality
• Other evidence
– Experimental reversibility7,122-133
– Relationship between strength improvements and pain and disability
improvement8,133
– Prospective strengthening reduces LBP risk 134-136

11. “…in none of these studies were
any mechanisms offered up to
explain how “normal” paraspinal
muscle could “dysfunction” to
predispose to LBP.” 87

12. Evolution?
“Nothing in biology makes sense except in the
light of evolution” 137

13. • Ancestral Health
• Westona A. Price138
• ‘Diseases of Civilisation’?
– WHO rank neck and back disorders highly as cause
of morbidity worldwide139
– Related to income & urbanisation140
– LBP slightly more common developing countries141
Development of the Hypothesis

14. Traditional Populations
• Hunter Gatherer/Indigenous Peoples Romanticism?
– Sure they are relatively free from138,142,143
• Obesity
• Cancer
• Heart disease
• Metabolic syndrome
• Etc.
• What about low back pain?
– Absence of evidence does not mean evidence of absence

15. Human Locomotion and LBP
• Mismatch Hypothesis
• Dual level control144,145
– Cultural evolution
– Biological evolution
• Locomotion Culture – Stabilised Spine146-150
– Dancing
– Working
– Walking
From Anderson145

16. • Australian Aborigines151-153
– 4.3% point prevalence
– 39% point prevalence
– 64% 7 week prevalence
– ~19% lifetime prevalence (sig higher than
non Indigenous ~17%)
• Sami Reindeer Herders154-155
– ~35% Men, ~60% Women 1 week
prevalence
– 60% 12 month prevalence (no assc. with
work)
• Maasai (compared to matched
Norwegians)156 (Wilhelmsen et al., 2007)
– Subjective Health Complaints sig greater
in Maasai (p = 0.002)
– 43% & 40% respectively 30 day prevalence
• New Guinea Highlander’s157
– 75% point prevalence
• Rural Chinese158
– 64% 12 month prevalence (Ass with
physical exposures i.e. farming)
• Rural Thai159,160
– ~8% lifetime prevalence
– ~1% 30 day prevalence
• Thai Farmers161
– 49% point prevalence
– 56% 12 month prevalence
– 77% lifetime prevalence
– Trunk extension endurance sig less
compared to asymptomatic162
• Rural Indonesians163
– Rural – 15.25%
– Urban – 22.5%
• Rural Malaysians164
– 11.6%
• Rural Philippines‘165
– 14.4%

17. • Studies with low prevalence
– Less inclination to report pain166
• 50% Australian Aborigines suffered low back pain but did not make this public167
– Most rural Thai/Malaysians/ Philippines' do not utilise health care – prefer to self
medicate164,168,169
• Indigenous/Traditional Healing?
– Finnish bonesetters subjectively better than drugs or Physical therapy170
– Native American Indians/Alaskan Natives171
• Subjective reports good
• SF36 sig worse in traditional healing users (p < 0.05)
• LBP associated with use (p < 0.05)

18. • Evidence of lumbar spine damage/degeneration in:
– Homo heidelbergensis172
– Homo erectus173
– Early Egyptian and Nubian remains174
– Ötzi the Iceman175
• So is it cultural (i.e. our lifestyles etc.)?

19. • Walking not causally associated with CLBP176
– Thus gait abnormality is likely a symptom
• Gait in CLBP
– Slower velocity
– Excessive hip, knee and ankle movement177
• The Spinal Engine178
Role of the Lumbar Spine in Gait
From Gracovetsky178

20. • Locomotion is the translation of CoG through space with least
energy expenditure179
– 3/6 major determinants relate to lumbopelvic motion
• Lumbar spine movement relate to identifiable gait events180
– Fine control, small displacements181-184
• Normal lumbar movement in gait
– Consistent waveform pattern180,183-185
– Sagittal and Frontal plane movement patterns consistent
between trials183,184,186

21. • Such fine control undoubtedly aided by
musculature181,185,187
• BUT….
• Deconditioning of Lumbar Extensors associated with
CLBP
– Reduced strength/endurance, CSA, fatigability
From Callaghan et al.185

22. • In those with LBP
– Poor adaptability trunk/pelvis co-ordination9,11-13,188,189
– Stride to stride variability in all planes190
• Particularly frontal plane11,190
– Poor lumbar extensor activity adaptability10,12
– Our research shows sig correlation between ILEX and
lumbar control during gait (under review)
• (r = -0.411; p = 0.029)

23. The Emergence of Bipedalism
• Early specialisation for Arboreal
Quadrupedalism in basal forms
– Wooly Opossums191
– Squirrel Monkeys 192
– Plesiadapis, Necrolemur193
• Arboreal Quadrupedalism 194, Leaping,
Climbing, Brachiation
– Catarrhini /Hominoidea- Old World Monkey’s195-197
– Early Miocene Apes - Proconsul/Morotopithecus198-202
• Semi-Terrestrial Quadrupedalism 194,203,
Climbing, Brachiation, Bridging, Knuckle
Walking
– Hominidae - Great Apes 194,203,204
– Late Miocene Apes – Dryopithecus/Morotpithecus 193,198,201,205
• Some Bipedalism, Climbing
• Habitual Bipedalism
– Hominini/Homo – Bipedal Great Apes
Oreopithecus/Ramapithecus/Ardipithecus/Australopithecus/H
omo193,206-210
From Nakatsukasa211

24. Changes in Lumbar/Pelvic Structure
• Lumbar Vertebrae
– Number
• 6 to 7
– Proconsul/Nachalopithecus/Morotopithec
us/OWMs/Gibbons 199,200,212,213
• 3 to 4
– Nachalopithecus/Morotopithecus/Dryopit
hicines /Great Apes202,213-215
• 5 to 6?
– Oreopithecus/Ardipithecus/Australopithec
us/Homo210,215,216
– Structure
• Craniocaudally elongate, ventral transverse
process
– Proconsul/Nachalopithecus/Morotopithec
us/Pieralopithecus/OWMs/Gibbons
200,214,217
• Craniocaudally shorter, posterior transverse
process
– Nachalopithecus/Morotopithecus/Dryopith
icines /Great Apes 213,218,219
• Loss of styloid process
– Morotopithecus/Oreopithecus/Ardipi
thecus/Australopithecus/Homo218-219
Classic drawings of
backs from Adolph
Schultz From Filler218

25. • Pelvis
– Narrow, laterally facing iliac blades
• Proconsul/OWMs/Gibbons200
– Lengthening of ilia with low lumbar
entrapment
• Morotopithecus/Dryopithecus
201,205,210,213
– Reduction in ilia with broadening and
anterior angling, broadening of sacrum
• Oreopithecus/Ardipithecus/Australopithe
cus/Homo 2206-208,210
• Invagination of spinal column220,221
From Filler218 From Lovejoy220

26. Changes in Lumbar/Hip Musculature
• Lumbar Musculature
– Large CSA
• Pronograde Arboeal Quadrupeds
199,200,222
– Reduced CSA, Iliocostalis situated
laterally
• Orthograde Semi-Terrestrial
Quadrupeds218,223
– Small CSA, PSIS posteriorly angled
(increased moment)
• Habitual Bipeds218,223
• Hip Musculature
– Glutei, Hamstrings220,222,224
• Quadrupeds –
Pronograde/Orthograde
– BHBK
• Fatiguing due to poor hip
leverage225
• Short backed
primates/OWM’s
– Except ‘trained’
Macaques211
• Spinal Changes occurred first?
– Retain hip ‘extensors’ 224,226
• Habitual Bipeds walking &
Running
– Gluteus Maximus
controls HAT
– Hamstrings control
swing phase
From Lovejoy220 From Lovejoy228

27. Conceptualising the Hypothesis
• Considering Dual Level Control
• Cultural/Environmental Influence – ‘Mismatch’?
– Unlikely - LBP common among nearly all observed
human populations
• Or - Biological Constraints?
– More Probable – The lumbar spine and pelvis
bears the compromise of adaptation to bipedality
• Long and flexible with relatively weak lumbar
musculature

28. Problems with the Hypothesis
• If LBP were a result of evolution - ‘Natural Selection would have take its toll.’
– Assumptions are:
• The presence of LBP would have had to negatively impact upon reproductive success
• This would have had to have been greater than the positive impact of being habitual
bipedalism
– But LBP can occur earlier than reproductive age (~10 years)227
– Also some adaptations appear to have occurred subsequent to bipedalism
• Increased posterior location of PSIS218-228
• Increased vertebral CSA173
• Common areas of debate in evolutionary anthropology
– Stages of Locomotion not completely agreed upon203,211,221
– Debated short backed or long backed LCA206-208,213,215,216,221,229
– Corresponding locomotion changes both have support213,230

29. What it Could Explain
• Why LBP is so widespread among human populations
• Deconditioning’s association with LBP
• Difficulty in conditioning the lumbar extensors231-239
– Most activities and ‘low back’ exercise are poorly effective
– Removal of hip extensors contribution required

30. What it Would Predict
• Expect to see lower prevalence of lumbar spine deficiencies
in:
– Extant non-hominid primates
• Apes & Monkeys free of spondylolysis228
• Chimpanzees, Bonobos, Gorilla significantly lower lumbar spine
degeneration240
– Extinct non-hominid primates?

31. Conclusions
• LBP is a multifactorial condition prevalent across most human populations
• Deconditioning of the lumbar extensor musculature is a consistent risk
factor for LBP
• The lumbar extensors are intrinsically involved in controlling human gait
• The emergence of bipedalism and evolution of the lumbar spine may have
resulted in a compromise
– Long flexible lumbar spine
– Relatively weak lumbar extensors
– Relatively strong hip extensors
• This may contribute to deconditioning of the lumbar extensors and thus
LBP and its associated symptoms.

32. Thank you for Listening
Any Questions?
…?